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cardio.nstemi.type2.v1

Type-2 MI (demand ischemia, no plaque rupture)

cardiologyacuteadultacuteinpatienttransitionoutpatient
Start encounter →Print handoutPRODUCTION

Phase E variant of cardio.nstemi.core.v1 — narrowed to type-2 MI per 4th UDMI 2018 (Thygesen Circulation 2018 PMID 30153967): troponin rise from supply-demand mismatch, NOT primary plaque rupture. Inverts the parent regimen — antiplatelet ONLY if known obstructive CAD; statin ONLY if known CAD; cath deferred unless obstructive CAD known + ongoing ischemia after trigger correction. Treat the trigger first per ACC/AHA 2025. Type-2 MI has higher 1-yr mortality than type-1 NSTEMI (37% vs 28% per DeFilippis PMID 30689349) but driven by underlying systemic disease (sepsis, anemia, multimorbidity), not by deferred antithrombotic strategy. Comorbidity optimisation is the dominant prognostic lever. Re-classification monitoring: new dynamic ECG OR clinical ACS syndrome → escalate to type-1 NSTE-ACS pathway (high-risk or intermediate-risk engine). Cocaine + chest pain → cocaine_chest_pain pathway (AVOID β-blocker per AHA 2008). Status INTEGRATED authored 2026-05-14 by shard-06-cardio-acute as part of the Phase E NSTEMI-by-stratum batch.

Entry points (5)

  • lab_abnormality
    hsTn rise/fall in patient with sepsis, severe anemia, tachyarrhythmia, hypoxia, hypotension, severe HTN, or drug toxicity (4th UDMI 2018)
    hstn_rise_with_supply_demand_mismatch
  • symptom
    hsTn elevation WITHOUT ischemic ECG and without clinical ACS syndrome — supports type-2 vs type-1
    no_ischemic_ecg_no_clinical_acs_syndrome
  • history
    Sepsis or septic shock with hsTn rise — most common type-2 trigger; treat sepsis bundle first per SSC 2026
    sepsis_or_septic_shock_with_troponin_rise
  • history
    AF with RVR / SVT / sinus tachycardia >150 with hsTn rise — rate control first
    tachyarrhythmia_with_demand_ischemia
  • lab_abnormality
    Hgb <7 (or <8 with cardiac symptoms) + hsTn rise — transfuse to MINT threshold first
    severe_anemia_or_acute_blood_loss_with_troponin

Required inputs (13)

  • agerequired
    demographic • used at CONTEXT
    Type-2 MI commoner in elderly + multimorbid; comorbidity-driven prognosis per DeFilippis PMID 30689349
  • sbprequired
    vital • used at RED_FLAGS
    Hypotension itself a trigger (decreases coronary perfusion); also gates whether this is type-2 vs type-1 with cardiogenic shock
  • hrrequired
    vital • used at CONTEXT
    Tachyarrhythmia trigger identification; rate control is primary therapy
  • temprequired
    vital • used at CONTEXT
    Sepsis screening — most common type-2 trigger
  • spo2required
    vital • used at CONTEXT
    Hypoxia trigger identification (e.g., COPD exacerbation, severe pneumonia, PE)
  • hs_troponin_serialrequired
    lab • used at INITIAL_WORKUP
    0/1-h or 0/3-h ESC 2023 algorithm — pattern in type-2 typically slow rise/plateau without sharp peak; distinguishes from type-1 acute coronary thrombus
  • cbcrequired
    lab • used at INITIAL_WORKUP
    Hgb identifies anemia trigger; WBC for sepsis trigger; platelets for HIT/DIC
  • lactaterequired
    lab • used at INITIAL_WORKUP
    Sepsis / shock screening — drives source-control timing
  • creatinine_egfrrequired
    lab • used at INITIAL_WORKUP
    Baseline kidney function — many type-2 triggers (sepsis, hypotension) cause concurrent AKI per KDIGO 2026
  • ecg_serialrequired
    imaging • used at INITIAL_WORKUP
    Confirm absence of ischemic ECG; detect sinus tachycardia / AF with RVR / strain pattern (PE)
  • cxrrequired
    imaging • used at INITIAL_WORKUP
    Pneumonia, edema, PTX, dissection screen — many trigger sources
  • known_cad_historyrequired
    history • used at CONTEXT
    Known obstructive CAD changes management — selective cath if ongoing ischemia post-trigger correction per ACC/AHA 2025
  • cocaine_methamphetamine_use
    history • used at CONTEXT
    Sympathomimetic toxicity is a type-2 trigger; cocaine chest pain has unique workflow per AHA 2008

12-phase flow (12)

  1. 1FRAME
    Confirm type-2 MI per 4th UDMI 2018 PMID 30153967 — hsTn rise from supply-demand mismatch (sepsis, anemia, tachyarrhythmia, hypoxia, hypotension, severe HTN, drug toxicity) WITHOUT ischemic ECG, WITHOUT clinical ACS syndrome, WITHOUT plaque-rupture imaging
    inputs: ecg_serial, hs_troponin_serial
    advance: Type-2 vs type-1 distinction documented; trigger identified
  2. 2ENTRY
    Triage with 0/1-h hsTn + ECG; prioritize trigger workup (sepsis bundle, transfusion, rate control, BP control, oxygen) over ACS pathway
    inputs: age
    advance: Trigger workup initiated
  3. 3CONTEXT
    Identify trigger (sepsis source, anemia cause, arrhythmia type, hypoxia source, HTN driver, drug toxicity); known CAD history gates downstream cath decision per ACC/AHA 2025
    inputs: sbp, hr, temp, spo2, creatinine_egfr, known_cad_history
    advance: Trigger and CAD context documented
  4. 4RED_FLAGS
    SBP <90 + lactate ≥4 → septic vs cardiogenic shock screening; sustained VT/VF → arrhythmia primary; new dynamic ECG → re-classify to type-1 NSTE-ACS pathway
    inputs: sbp
    actions: cardiogenic_shock, wide_complex_tach, cocaine_chest_pain
    advance: Shock differentiated; arrhythmia controlled if present
  5. 5INITIAL_WORKUP
    Serial ECG + hsTn (slow-rise pattern typical for type-2), CBC, BMP, lactate, lipase if abdominal, blood cultures + UA + CXR for sepsis source, BNP for HF differentiation
    inputs: ecg_serial, hs_troponin_serial, cbc, lactate, cxr
    actions: acs_pathway, panel.cardiac, panel.cbc, panel.renal
    advance: Trigger workup complete + type-1 ruled out
  6. 6BRANCHING_WORKUP
    Targeted: bedside echo for global hypokinesis (sepsis cardiomyopathy) vs RWMA (type-1 ACS); CT-PE if hypoxia + tachycardia; CT-A if dissection suspicion; defer stress/CCTA until trigger resolved
    actions: chest_pain, acute_valvular_emergency
    advance: Branch resolved
  7. 7DIFFERENTIAL
    Type-2 MI vs type-1 NSTEMI (plaque rupture) vs Takotsubo vs myocarditis vs strain (PE, severe HTN) per 4th UDMI 2018 PMID 30153967
    advance: Type-2 confirmed; type-1 deferred to NSTE-ACS pathway
  8. 8RISK_STRATIFICATION
    Type-2 MI 1-yr mortality 37% (vs type-1 28%) per DeFilippis 2019 PMID 30689349 — driven by comorbidity not coronary anatomy. HEART/TIMI/GRACE may underestimate; SCAI 2022 staging if hemodynamically unstable
    inputs: age, sbp, hr, creatinine_egfr, hs_troponin_serial
    actions: calc.heart, calc.grace, calc.ckd_epi_2021
    advance: Comorbidity-weighted risk documented
  9. 9TREATMENT
    Treat the trigger primarily — sepsis bundle (SSC 2026), rate control for tachyarrhythmia, transfuse to MINT threshold for anemia, oxygen if hypoxic, BP control for severe HTN, antidote for drug toxicity. Antiplatelet ONLY if known obstructive CAD; statin ONLY if known CAD per ACC/AHA 2025. Selective cath only if obstructive CAD known + ongoing ischemia after trigger correction
    inputs: creatinine_egfr, cbc
    advance: Trigger therapy initiated + CAD-driven antithrombotic decision documented
  10. 10DISPOSITION
    Setting driven by trigger severity — septic shock → ICU; AF with RVR + stable → telemetry; mild anemia + mild trop bump → general medicine + outpatient stress later
    advance: Trigger-appropriate disposition set
  11. 11MONITORING
    Serial hsTn to confirm trigger correction normalises trend; trend lactate, vitals, trigger-specific markers; re-screen ECG for new ischemic changes that would re-classify to type-1
    inputs: creatinine_egfr, cbc
    actions: panel.cardiac, panel.renal
    advance: Monitoring orders documented
  12. 12FOLLOWUP
    Outpatient cardiology + stress test or CCTA if recovers — to detect underlying obstructive CAD that contributed to demand-supply ischemia. Optimise comorbidities (sepsis recovery, HF, CKD, DM)
    advance: Outpatient cardiology + stress workup booked